Nd is responsible for a majority of IGF transport [53]. Because IGFBP3 has intrinsic IGF-binding activity that can act to sequester IGF from its cognate receptor [13], it is possible that using IGFBP3 as a therapeutic agent would be useful to GIST patients with abnormal IGF expression or IGF-dependent IGF-1R activation. Furthermore, if IGFBP3 is indeed acting through an IGF-dependent mechanism, a